| pubmed-article:20562447 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20562447 | lifeskim:mentions | umls-concept:C0012634 | lld:lifeskim |
| pubmed-article:20562447 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
| pubmed-article:20562447 | lifeskim:mentions | umls-concept:C0443147 | lld:lifeskim |
| pubmed-article:20562447 | lifeskim:mentions | umls-concept:C0205409 | lld:lifeskim |
| pubmed-article:20562447 | lifeskim:mentions | umls-concept:C1425223 | lld:lifeskim |
| pubmed-article:20562447 | lifeskim:mentions | umls-concept:C0232217 | lld:lifeskim |
| pubmed-article:20562447 | lifeskim:mentions | umls-concept:C1524003 | lld:lifeskim |
| pubmed-article:20562447 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:20562447 | pubmed:dateCreated | 2010-8-18 | lld:pubmed |
| pubmed-article:20562447 | pubmed:abstractText | Isolated cardiac conduction block is a relatively common condition in young and elderly populations. Genetic predisposing factors have long been suspected because of numerous familial case reports. Deciphering genetic predisposing factors of conduction blocks may give a hint at stratifying conduction block carriers in a more efficient way. | lld:pubmed |
| pubmed-article:20562447 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20562447 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20562447 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20562447 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:20562447 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20562447 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20562447 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:20562447 | pubmed:issn | 1942-3268 | lld:pubmed |
| pubmed-article:20562447 | pubmed:author | pubmed-author:KUOH YHY | lld:pubmed |
| pubmed-article:20562447 | pubmed:author | pubmed-author:MégarbanéAndr... | lld:pubmed |
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| pubmed-article:20562447 | pubmed:author | pubmed-author:BeckmannAlfA | lld:pubmed |
| pubmed-article:20562447 | pubmed:author | pubmed-author:KurtbayGüvenG | lld:pubmed |
| pubmed-article:20562447 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20562447 | pubmed:volume | 3 | lld:pubmed |
| pubmed-article:20562447 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20562447 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20562447 | pubmed:pagination | 374-85 | lld:pubmed |
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| pubmed-article:20562447 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20562447 | pubmed:articleTitle | Gain-of-function mutations in TRPM4 cause autosomal dominant isolated cardiac conduction disease. | lld:pubmed |
| pubmed-article:20562447 | pubmed:affiliation | Université de Lyon, Laboratoire Cardiogénétique, Equipe d'Accueil 4171, Lyon, France. | lld:pubmed |
| pubmed-article:20562447 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20562447 | pubmed:publicationType | Case Reports | lld:pubmed |
| pubmed-article:20562447 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:54795 | entrezgene:pubmed | pubmed-article:20562447 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:20562447 | lld:entrezgene |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:20562447 | lld:pubmed |
